Why the study?
Post-MI replacement fibrosis can lead to left ventricular remodeling and heart failure, with microRNAs significantly contributing to the modulation of involved signaling pathways.
MicroRNAs play a significant role in modulating signaling pathways involved in post-myocardial infarction left ventricular remodeling and hold potential as prognostic biomarkers for heart failure.
TGF-β pathways drive post-MI fibrosis and LVR; leaves open diagnostic tools to identify high-risk patients before HF develops.
Myocardial infarction (MI) is one of the most frequent cardiac emergencies, with significant potential for mortality. One of the major challenges of the post-MI healing response is that replacement fibrosis could lead to left ventricular remodeling (LVR) and heart failure (HF). This process involves canonical and non-canonical transforming growth factor-beta (TGF-β) signaling pathways translating into an intricate activation of cardiac fibroblasts and disproportionate collagen synthesis. Accumulating evidence has indicated that microRNAs (miRNAs) significantly contribute to the modulation of these signaling pathways. This review summarizes the recent updates regarding the molecular mechanisms underlying the role of the over 30 miRNAs involved in post-MI LVR. In addition, we compare the contradictory roles of several multifunctional miRNAs and highlight their potential use in pressure overload and ischemia-induced fibrosis. Finally, we discuss their attractive role as prognostic biomarkers for HF, highlighting the most relevant human trials involving these miRNAs.
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Maries et al. (2021) studied this question.
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